Abstract
Tuberculosis remains a major health problem. Mycobacterium tuberculosis, the causative agent of tuberculosis, can replicate and persist in host cells. Noncoding RNAs (ncRNAs) widely participate in various biological processes, including Mycobacterium tuberculosis infection, and play critical roles in gene regulation. In this review, we summarize the latest reports on ncRNAs (microRNAs, piRNAs, circRNAs and lncRNAs) that regulate the host response against Mycobacterium tuberculosis infection. In the context of host-Mycobacterium tuberculosis interactions, a broad and in-depth understanding of host ncRNA regulatory mechanisms may lead to potential clinical prospects for tuberculosis diagnosis and the development of new anti-tuberculosis therapies.
Highlights
Tuberculosis (TB), which is caused by the intracellular pathogen Mycobacterium tuberculosis (M. tuberculosis), remains the leading cause of death from a single infectious agent
Taganov et al showed that miR-146 regulates the immune response by controlling Toll-like receptor 4 (TLR4) and cytokine signaling in monocyte ThP-1 cells induced by lipopolysaccharide (LPS) to protect host cells from excessive inflammation in an NF-kB dependent manner [16]
Subsequent studies established miRNA regulation upon bacterial infection as a common phenomenon, with implications for multiple host cell functions ranging from autophagy and modulation of immune responses involved in signaling pathways, cell cycle and cell apoptosis
Summary
Tuberculosis (TB), which is caused by the intracellular pathogen Mycobacterium tuberculosis (M. tuberculosis), remains the leading cause of death from a single infectious agent (ranking higher than HIV/AIDS). The main reasons are that M. tuberculosis rapidly exhibits drug-resistant mutations under the pressure of antibiotics and that the development of new TB vaccines and effective anti-tuberculosis drugs is prolonged [2, 3] Another reason is that during the evolutionary processes involved in coexisting with the host for thousands of years, M. tuberculosis has evolved with a set of almost perfect immune escape mechanisms that enable M. tuberculosis to skillfully avoid the elimination and killing of the host immune system and ensure its survival in macrophages for a long time [4, 5]. The immune system initiates effective defense mechanisms, including cellular and humoral factors, when the host is attacked by pathogens such as bacteria, fungi and viruses [6] While proteins and their immunomodulatory properties have been extensively studied, the roles of noncoding RNAs (ncRNAs) in controlling host defense have not been completely elucidated We focus on the regulation of host ncRNAs involved in host-M. tuberculosis interactions
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